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DRASTIC CURES FOR OBESITY

OBESITY is chemically fairly simple and clinicallyappallingly difficult. Mayer 1 in Boston has shownclearly that the obese move less than the slender. Fat

girls can play a good game of tennis and stand motion-less for 50% of the time, while their slim competitorshop up and down. The genetic factor in obesity isreflected in the finding that the children of the obeseare much more liable to become fat than adopted child-ren in the same family. Moreover, a reduction in theamount of spontaneous movement has been observedin infants of obese families. 2,3 Added to this economyof movement are psychological and social pressures,with the outcome that food intake, measured in calories,is greater than calorie output-and obesity results.To keep a steady weight, calorie intake must be regu-lated to within 1 % of output, when output is measuredas heat plus urinary and fxcal loss.How the normal person regulates calorie intake so

that it is within 1 % of output is an unsolved mystery.Nor does the suggestion that the output of calories inthe urine can be varied help to clarify the situation,since this loss is normally only a small fraction of theintake and energy expenditure can range by a factor offive or more.4,5 But the social cost and cost to health s

of being obese are so great that patients will do almostanything to get rid of the burden of fat. The one thingthey find difficult is to eat less and move more.

Doctors are therefore tempted to apply drasticremedies. Dinitrophenol and tapeworms are out offashion. But prolonged total fasting has been in vogueand was found to be dangerous.7 A new report 8 showsthat the fatty liver of the obese may become slightlyworse on fasting, but return to a more normal low-calorie diet is accompanied by restitution of normalliver structure and function. Drenick et awl. show anadmirable piece of liver from a patient whom theypersuaded to achieve the weight of 202 lb. (92 kg.)from the astonishing starting-point of 473 lb. (215 kg.).When a small-bowel bypass was inserted into some oftheir patients, however, a severe fatty liver followed,and in one case cirrhosis of the liver was found at

necropsy. The extensive fatty change after bypass wasnot amenable to treatment by dietary vitamin supple-ments, and may have been caused by an inducedaminoacid imbalance. Very fatty livers have been

produced by means of such imbalanced diets.9 9

Jejuno-ileal shunts must thus join the list of dangerouscures for obesity. It is interesting to speculate whydoctors should impose a surgical operation designed toblock intestinal function on obese patients. Would

they cut the hand from a cigarette smoker ? It is notthe danger of obesity that launches the surgeon’s knife;perhaps it is the dependent personality asking for

punishment ?1. Bullen, B. A., Reid, R. B., Mayer, J. Am. J. clin. Nutr. 1964, 14, 211.2. Mayer, J. 8th International Congress of Nutrition, Prague, 1969.3. Eid, E. E. Br. med. J. April 11, 1970, p. 74.4. Durnin, J. V. G. A., Passmore, R. Work Energy and Leisure.

London, 1967.5. Pilkington, T. R. E., Gainsborough, H., Rosenoer, V. M., Cavey, M.

Lancet, 1960, i, 856.6. Office of Health Economics: Obesity and Disease. London, 1969.7. Garnett, E. S., Barnard, D. L., Ford, J., Goodbody, R. A.,

Woodhouse, M. A. Lancet, 1969, i, 914.8. Drenick, E., Simmons, F., Murphy, J. F. New Engl. J. Med. 1970,

282, 829.9. Sidransky, H., Verney, E. Archs Path. 1964, 78, 134.

Obesity is a risk undertaken voluntarily, like

smoking or pregnancy or oral contraception. As longas the patient understands the risks, and in this instanceis given every encouragement to reduce food intakeand increase activity, the doctor has performed hisproper function. It is not his job to increase the risksof the obese life with drastic cures.

NEUROLOGICAL COMPLICATIONS OF

TUBERCULOSIS

IN Garland and Armitage’s analysis 1 (published in1933) of 13,000 consecutive necropsies over twenty-three years, 3-4% of all the patients died of tubercu-lous meningitis. Tuberculomas constituted a third ofall cases of intracranial masses, and the proportionrose to two-thirds in children. Pott’s disease of thespine and its complication of paraplegia were alsocommon. Paraplegia might be sudden in onset, dueto vertebral collapse or endarteritic infarction of thecord, or more often subacute, due to compressionfrom extradural granulation tissue.2With the decline in tuberculosis in this country, the

incidence of all forms of neurological tuberculosis hasdecreased dramatically. Tuberculous meningitis isthe only complication seen with any frequency in theUnited Kingdom today, and its diagnosis and earlyeffective treatment remain a matter of urgency.Despite triple chemotherapy (isoniazid, P.A.s., and

streptomycin) the mortality-rate remains about 50%for patients admitted in coma, and 30% for thoseadmitted with drowsiness or focal signs in the centralnervous system,.3-6 The prognosis is worse in the veryyoung and the very old,3,5 and delay in startingeffective therapy worsens the prognosis.’ 7 The late

sequelae of tuberculous meningitis include mental

deficiency, epilepsy, hemiplegia, hypothalamic and

pituitary disturbances, blindness with optic atrophy,deafness, hydrocephalus and hydromyelia due to basalarachnoiditis, and paraplegia from spinal adhesivearachnoiditis. 4,5,8-13

Tuberculosis of the nervous system, however, hasbecome so uncommon in the United Kingdom that itis rarely the first diagnosis that comes to mind. In lessfortunate countries such as India and Pakistan, a fairlyrapidly developing spastic paraplegia will be treatedas tuberculosis until proved otherwise 14,15 (neoplasticcompression of the cord might be the first diagnosis1. Garland, H. G., Armitage, G. J. Path. Bact. 1933, 37, 461.2. Griffiths, D. L1., Seddon, H. J., Roaf, R. Pott’s Paraplegia. London,

1956.3. Fitzsimons, J. M. Tubercle, 1963, 44, 87.4. Wasz-Höckert, O., Dormer, M. Acta Pœdiat., Uppsala, 1963,

suppl. 141, 1.5. Falk, A. Am. Rev. resp. Dis. 1965, 91, 823.6. Hinman, A. R. ibid. 1967, 95, 670.7. Fitzsimons, J. M., Smith, H. Tubercle, 1963, 44, 103.8. Brooks, W. D. W., Fletcher, A. P., Wilson, R. R. Q. Jl Med. 1954,

23, 275.9. Todd, R. McC., Neville, J. G. Archs Dis. Childh. 1964, 39, 213.

10. Asherson, R. A., Jackson, W. P. U., Lewis, B. Br. med. J. 1965,ii, 839.

11. Gomez, A. J., Ziegler, D. K. J. nerv. ment. Dis. 1966, 142, 94.12. Summers, V. K., Hipkin, L. J., Hughes, R. O., Davis, J. C. Br.

med. J. 1968, i, 359.13. Appleby, A., Bradley, W. G., Foster, J. B., Hankinson, J.,

Hudgson, P. J. neurol. Sci. 1969, 8, 451.14. Wadia, N. H., Dastur, D. K. ibid. p. 239.15. Dastur, D. K., Wadia, N. H. ibid. p. 261.